Evidence map›Paper›PMID 22909100›Full record

ArticleNucleic acid therapeutics2012

Targeted p21WAF1/CIP1 activation by RNAa inhibits hepatocellular carcinoma cells.

Mika Kosaka, Moo Rim Kang, Glen Yang, Long-Cheng Li

Abstract read
In one paragraph

Article in Nucleic acid therapeutics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.6field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
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  7. Emerging Progress of RNA-Based Antitumor Therapeutics.International journal of biological sciences · 2023
    Review
  8. Article
  9. Article
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  19. Article
  20. Promoter-associated endogenous and exogenous small RNAs suppress human bladder cancer cell metastasis by activating p21 (CIP1/WAF1) expression.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Mika KosakaDepartment of Urology and Helen-Diller Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA, USA.
Moo Rim Kang
Glen Yang
Long-Cheng Li
University of California, San Francisco · US

Funding

Transcriptional Activation by Small RNA: Mechanism and Design RulesR01GM090293 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LI, HAO, LI, LONG-CHENG · 2009 to 2013
$2.3M
Small RNA targeted gene activation for the treatment of prostate cancerR21CA131774 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LI, LONG-CHENG · 2008 to 2009
$382k
NCI NIH HHS 1R21CA131774NIGMS NIH HHS 1R01GM090293-0109
6 · The paper itself

Abstract

RNA activation (RNAa) is a mechanism of gene activation triggered by promoter-targeted small double-stranded RNA (dsRNA), also known as small activating RNA (saRNA). p21(WAF1/CIP1) (p21) is a putative tumor suppressor gene due to its role as a key negative regulator of the cell cycle and cell proliferation. It is frequently downregulated in cancer including hepatocellular carcinoma (HCC), but is rarely mutated or deleted, making it an ideal target for RNAa-based overexpression to restore its tumor suppressor function. In the present study, we investigated the antigrowth effects of p21 RNAa in HCC cells. Transfection of a p21 saRNA (dsP21-322) into HepG2 and Hep3B cells significantly induced the expression of p21 at both the mRNA and protein levels, and inhibited cell proliferation and survival. Further analysis of dsP21-322 transfected cells revealed that dsP21-322 arrested the cell cycle at the G(0)/G(1) phase in HepG2 cells but at G(2)/M phase in Hep3B cells which lack functional p53 and Rb genes, and induced both early and late stage apoptosis by activating caspase 3 in both cell lines. These results demonstrated that RNAa of p21 has in vitro antigrowth effects on HCC cells via impeding cell cycle progression and inducing apoptotic cell death. This study suggests that targeted activation of p21 by RNAa may be explored as a novel therapy for the treatment of HCC.

Indexed as

Transcriptional ActivationApoptosisCarcinoma, HepatocellularCaspase 3Cell Cycle CheckpointsCell ProliferationCell SurvivalCyclin-Dependent Kinase Inhibitor p21Hep G2 CellsHumansRNA, Double-StrandedCASP3 protein, humanCaspase 3CDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21RNA, Double-Stranded

Identifiers

PMID22909100
PMCPMC3464408
OpenAlexW239839785

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.